MicroRNA-132 modifies angiogenesis in patients with ischemic cerebrovascular disease by suppressing the NF­κB and VEGF pathway.

ABSTRACT

In the present study, the expression of microRNA (miR)­132 and the mechanism by which it modifies angiogenesis in patients with ischemic cerebrovascular disease (ICD) was investigated. RNA isolation and reverse transcription­quantitative polymerase chain reaction were used to measure miR­132 expression in patients with ICD. Inflammatory factors were measured using ELISA kits and western blotting measured B­cell lymphoma­2 (Bcl­2)­associated X/Bcl­2 ratio (Bax/Bcl­2 ratio), nuclear factor (NF)­κB p65, matrix metalloproteinase­9 (MMP­9), vascular cell adhesion molecule­1 (VCAM­1) and protein expression of inducible nitric oxide synthase (iNOS), and vascular endothelial growth factor (VEGF) protein expression. miR­132 expression in patients with ICD was lower compared with healthy volunteers. PC12 cells were used to create an oxygen glucose deprivation (OGD) model. miR­132 overexpression in an in vitro model was able to reduce tumor necrosis factor­a, interleukin (IL)­1ß, IL­6, IL­8, cyclooxygenase­2, caspase­3 and caspase­9 levels, suppress Bax/Bcl­2 ratio, NF­κB p65, MMP­9, VCAM­1, iNOS, VEGF protein expression. The results suggested that miR­132 may modify angiogenesis in patients with ICD by suppressing the NF­κB pathway and promoting the VEGF pathway, and may develop into a therapy for ICD in future research.